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. Author manuscript; available in PMC: 2024 Mar 15.
Published in final edited form as: Cell Rep. 2024 Jan 23;43(2):113700. doi: 10.1016/j.celrep.2024.113700

Figure 7. AA inhibits PKC, PKD, and JNK.

Figure 7.

(A and B) Cell death (A) and IL-1β production (B) in THP-1 cells primed with LPS (200 ng/mL, 3 h) followed by stimulation with nigericin (10 μM, 1 h) in presence of PKC inhibitor (sotrastaurin, 10 μM), PKD inhibitor (CRT006601, 10 μM), JNK inhibitor (SP600125, 10 μM), AA (40 μM), or LCA (30 μM).

(C and D) Immunoblots (C) and densitometric quantification (D) of THP-1 cells primed with LPS (200 ng/mL, 3 h) and stimulated with nigericin (10 μM) in presence of AA (40 μM) or LCA (30 μM) for up to 60 min.

(E and F) Cell death (E) and IL-1β production (F) in THP-1 cells primed with Pam3CSK4 (200 ng/mL, 4 h) followed by stimulation with PA (500 μM, 16 h) in presence of PKC inhibitor (sotrastaurin, 10 μM), PKD inhibitor (CRT006601, 10 μM), JNK inhibitor (SP600125, 10 μM), AA (40 μM), or LCA (30 μM).

(G and H) Quantification of p-JNK (G) and nuclear p-c-Jun (H) in THP-1 cells primed with Pam3CSK4 (200 ng/mL, 4 h) after stimulation with PA (500 μM, 24 h) in presence of 40 μM AA.

THP-1 cells were differentiated with PMA (200 ng/mL) for 24 h followed by 24 h washout prior to the experiments. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001 in comparison to nigericin-treated cells (A and B) or PA-treated cells (E and F) unless indicated otherwise (one-way analysis of variance with Tukey’s multiple comparison test). n.s., not significant. Data are from three (C and D), four (A, B, E, and F), or five (G and H) independent experiments (mean and SEM).